ArticleCirculation research2020
PKG1α Cysteine-42 Redox State Controls mTORC1 Activation in Pathological Cardiac Hypertrophy.
Article in Circulation research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 45 citations in OpenAlex.
- LAT1/SLC7A5-mediated amino acid uptake is regulated by redox signals triggered by formyl-peptide receptor 2.The FEBS journal · 2026Article
- mTORC1 and nuclear ERK spatially control translation in cardiomyocytes through 4EBP1 phosphorylation.Science signaling · 2026Article
- 4E-BP inhibition ameliorates heart failure through translational upregulation of SERCA2a and modulation of mitochondrial redox signaling in cardiomyocytes.Redox biology · 2026Article
- Redox-dependent activation of protein kinase G1α contributes to transient receptor potential cation channel subfamily V member 1-mediated acute nociceptive pain behavior.Redox report : communications in free radical research · 2025Article
- Extracellular mitochondria contribute to acute lung injury via disrupting macrophages after traumatic brain injury.Journal of neuroinflammation · 2025Article
- Promoting proteostasis by cAMP/PKA and cGMP/PKG.Trends in molecular medicine · 2025Review
- Cardiac cGMP Regulation and Therapeutic Applications.Hypertension (Dallas, Tex. : 1979) · 2025Review
- Phosphodiesterases: Evolving Concepts and Implications for Human Therapeutics.Annual review of pharmacology and toxicology · 2025Review
- Activation of AHR by ITE improves cardiac remodelling and function in rats after myocardial infarction.ESC heart failure · 2023Article
- Regulation of mTOR Signaling: Emerging Role of Cyclic Nucleotide-Dependent Protein Kinases and Implications for Cardiometabolic Disease.International journal of molecular sciences · 2023Review
- Vps4a Regulates Autophagic Flux to Prevent Hypertrophic Cardiomyopathy.International journal of molecular sciences · 2023Article
- Potential Role of the mTORC1-PGC1α-PPARα Axis under Type-II Diabetes and Hypertension in the Human Heart.International journal of molecular sciences · 2023Article
- Indirect epigenetic testing identifies a diagnostic signature of cardiomyocyte DNA methylation in heart failure.Basic research in cardiology · 2023Article
- The Importance of mTORC1-Autophagy Axis for Skeletal Muscle Diseases.International journal of molecular sciences · 2022Review
- Actin-Binding Proteins in Cardiac Hypertrophy.Cells · 2022Review
- Ca2+/calmodulin-dependent protein kinase II and protein kinase G oxidation contributes to impaired sarcomeric proteins in hypertrophy model.ESC heart failure · 2022Article
- Single serine on TSC2 exerts biased control over mTORC1 activation mediated by ERK1/2 but not Akt.Life science alliance · 2022Article
- Induction of apoptosis and autosis in cardiomyocytes by the combination of homocysteine and copper via NOX-mediated p62 expression.Cell death discovery · 2022Article
- mTOR inhibitor improves testosterone-induced myocardial hypertrophy in hypertensive rats.The Journal of endocrinology · 2022Article
- The complex network of mTOR signalling in the heart.Cardiovascular research · 2022Review
Corrections and comments
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Authors and funding
13 authors at 1 institution in 2 countries.
Funding
Abstract
rationaleStimulated PKG1α (protein kinase G-1α) phosphorylates TSC2 (tuberous sclerosis complex 2) at serine 1365, potently suppressing mTORC1 (mechanistic [mammalian] target of rapamycin complex 1) activation by neurohormonal and hemodynamic stress. This reduces pathological hypertrophy and dysfunction and increases autophagy. PKG1α oxidation at cysteine-42 is also induced by these stressors, which blunts its cardioprotective effects.
objectiveWe tested the dependence of mTORC1 activation on PKG1α C42 oxidation and its capacity to suppress such activation by soluble GC-1 (guanylyl cyclase 1) activation. METHODS AND
resultsCardiomyocytes expressing wild-type (WT) PKG1α (PKG1α
conclusionsOxidation of PKG1α at C42 reduces its phosphorylation of TSC2, resulting in amplified PO-stimulated mTORC1 activity and associated hypertrophy, dysfunction, and depressed autophagy. This is ameliorated by direct GC-1 stimulation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.